DOACs are also known as novel or non-vitamin K anticoagulants (NOAC). However, there is a possibility that a healthcare professional might mistake NOAC for ‘no anticoagulants’ with potentially serious or even life-threatening consequences.44 So, this Learning Zone uses DOAC.
For eligible AF patients, the ESC/EHRA guidelines recommend a DOAC in preference to a warfarin or another vitamin K antagonist. The guidelines also recommend DOACs rather than a vitamin K antagonist or aspirin in AF patients who experienced a previous stroke. However, the guidelines do not recommend DOACs for patients with mechanical heart valves or moderate-to-severe mitral stenosis, where warfarin is the preferred oral anticoagulant.5
In contrast to warfarin, DOACs are highly specific and show a relatively high affinity for a single enzyme in the coagulation cascade.42 Apixaban, edoxaban and rivaroxaban directly inhibit factor Xa, thereby disrupting the intrinsic and the extrinsic pathways (Figure 19) and preventing thrombin formation.7,40 Dabigatran etexilate directly inhibits thrombin.40
DOACs bind to the active site of the enzymes involved in the coagulation cascade and so compete with the normal substrates. Importantly, DOACs do not completely inhibit the enzyme, which means a strong procoagulant stimulus can overcome the anticoagulant effect.42 This property might explain why the risk of intracranial haemorrhage seems to be lower with some DOAC than with warfarin. The brain is rich in tissue factor, a potent stimulus for coagulation. Exposure of blood to brain tissues could, therefore, overcome DOAC inhibition.42Discover pharmacokinetics and pharmacodynamics of direct oral anticoagulants in the next section
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